Goroll_Primary Care Medicine, 8e

SECTION XIV Ear, Nose, and Throat Problems

Chapter 211

SCREENING FOR ORAL CANCER EDWARD T. LAHEY III

T here are estimated to be at least 23,000 new cases of oral cancer diagnosed each year in the United States, with oral cancer causing more than 5,000 deaths yearly. The anatomi cal borders within which oral cancer occurs are the lips, oral tongue (the portion in front of circumvallate papillae), buccal and alveolar mucosae, floor of mouth, and hard palate. Oral cancer is distinct from oropharyngeal cancer (cancer of the soft palate, tongue base, tonsils, and pharyngeal walls) with regard to risk factors and natural history though in both anatomic areas, squamous cell carcinoma represents more than 90% of diagnosed malignancies. This chapter focuses predominantly on oral cancer but includes some consideration of oropharyn geal malignancy since it may present in the oral cavity. Despite the ready accessibility of the oral cavity to inspec tion by physicians, dentists, and patients, 50% of oral cancers have already metastasized at the time of initial diagnosis due to early lesions usually being painless and often going undetected during routine care visits. There is a precipitous decline in prognosis once oral cancer has progressed beyond early, local ized disease, so the primary care physician can play an impor tant role in early detection. Counseling patients on prevention is another responsibility, given that 90% of oral cancer cases are linked to alterable risk factors. EPIDEMIOLOGY AND RISK FACTORS (1–7) More than 97% of oral cancers occur among patients older than 35 years of age, with a peak incidence in the sixth decade for women and fifth decade for men. Demographically, black men have the highest risk of developing oral cancer. Risk factors include increased age , smoking and alcohol abuse, history of previ ous cancer of the upper aerodigestive tract, and chronic immu nocompromise . While the precise etiology of oral cancer remains unknown, many of these risk factors probably act as cocarcino gens and/or immunosuppressants, effecting malignant change or reducing immune response in concert with some primary factor not yet elucidated. Increased chromosomal fragility has been found in nonsmokers who develop oral cancers. Tobacco and alcohol abuse warrant special attention in that they are synergistic cocarcinogens. It is theorized that the solvent effect of alcohol allows better penetration of tobacco-associated carcinogens (especially tobacco-specific nitrosamines) into the oral mucosa. Topical application by chewing or dipping tobacco or snuff (pressing it up against the cheek and gums) is believed to enhance such risk, though data are mixed, probably due in part to differences in preparations and patterns and duration of use. Patients with a history of combined tobacco and alcohol abuse often present with multiple dysplastic and malignant lesions due to “field cancerization.” Nonsmoking oral cancer

patients are more likely to present at the extremes of age with lesions of the lateral borders of the tongue and rarely develop cancer of the floor of the mouth. Mucosal atrophy increases the risk of oral cancers. Chronic iron deficiency leading to Plummer-Vinson syndrome alters mucosal tissues, which might account for the increased incidence of oral carcinoma associated with the condition. The atrophic glossitis of tertiary syphilis might account for the increased incidence of tongue cancer associated with the condition. The use of betel quid , a stimulant composed of a betel leaf combined with areca nut and/or tobacco and placed between the lip/cheeks and gingiva, is common among natives of Southeastern Asia and is another well-established risk factor for oral cancer. Chronic irritation of the oral mucosa by ill-fitting dentures, poorly restored teeth, or particularly spicy diets has often been mentioned as contributing to the development of oral carcinoma; however, no epidemiologic data support this view. Topical oral use of a smokeless tobacco preparation (e.g., chewing, dipping, or snuff) is detrimental to oral and systemic health and, as noted, may enhance risk for oral cancer. Human papilloma virus (HPV) is an important risk factor for oropharyngeal cancer (see later discussion) but is less well established as a risk factor for oral cancer, identified in 0% to 10% of oral cancer tumors. Overall incidence is increasing due to the rise in sexually trans mitted oral HPV infection. HPV-positive disease (especially that involving the HPV-16 strain) now accounts for as much as 42% to 87% of cases. Epidemiologic study has been help ful in identifying high-risk groups. It finds oral HPV infection significantly higher among men than women and especially high in those with more than 16 lifetime sexual partners, smok ing more than 20 cigarettes/day, men who have sex with men, many lifetime oral sexual encounters, and men with concurrent HPV infection. These squamous cell cancers constitute at least two distinct clinicopathologic entities related to their risk factors. Those associated with smoking and alcohol excess demonstrate a worse prognosis and greater refractoriness to treatment than HPV positive disease. Epidemiologic evidence finds little interaction between HPV-positive and HPV-negative disease, suggesting separate disease mechanisms, although smoking worsens the prognosis for both. Risk Factors for Lip Cancer Cancer of the lip has a risk factor profile more similar to that of skin cancer. Incidence is particularly high among fair-skinned Epidemiology and Risk Factors for Oropharyngeal Cancer

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